Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 384, Issue 4, Pages 524-529Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2009.05.015
Keywords
Amyotrophic lateral sclerosis (ALS); L-Arginine; Motor neuron; Polyamines; Superoxide dismutase 1 (SOD1)
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Funding
- NIA NIH HHS [P30 AG013846, P30 AG013846-09, P30 AG13846] Funding Source: Medline
- NINDS NIH HHS [NS52724, R01 NS052724-03, R01 NS052724] Funding Source: Medline
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Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by progressive paralysis due to motor neuron degeneration. Despite the fact that many different therapeutic strategies have been applied to prevent disease progression, no cure or effective therapy is currently available for ALS. We found that L-arginine protects cultured motor neurons from excitotoxic injury. We also found that L-arginine supplementation both prior to and after the onset of motor neuron degeneration in mtSOD1 (G93A) transgenic ALS mice significantly slowed the progression of neuropathology in lumbar spinal cord, delayed onset of motor dysfunction, and prolonged life span. Moreover, L-arginine treatment was associated with preservation of arginase I activity and neuroprotective polyamines in spinal cord motor neurons. Our findings show that L-arginine has potent in vitro and in vivo neuroprotective properties and may be a candidate for therapeutic trials in ALS. Published by Elsevier Inc
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